Protective Effects of Clarithromycin, a Lipophilic 14-membered Macrolide, on Hemolysis Induced by Lysophosphatidylcholine in Human Erythrocytes
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We examined the effects of 8 macrolide antimicrobial agents, including 14-, 15- and 16-membered ring lactone and ketoride derivatives, on hemolysis induced by lysophosphatidylcholine (LPC) in human erythrocytes. LPC induced hemolysis at concentrations above the critical micelle concentration (4 µM). Vitamin E (α-tocopherol), used as a reference drug, attenuated the 50% hemolysis induced by 6 µM LPC when present at concentrations between 1 µM and 100 mM. Clarithromycin significantly attenuated LPC-induced hemolysis at a wider range of concentrations (100 nM to 1 mM), but other macrolides attenuated hemolysis only at high concentrations (100 µM and/or 1 mM). Since vitamin E tends to stabilize membranes due to its high lipophilicity, it appears that the high lipophilicity of clarithromycin is responsible for its protective action against damage induced by LPC. However, rokitamycin was not effective, although it is more lipophilic than clarithromycin, indicating that factors other than high lipophilicity are responsible for the protective effects of macrolide antimicrobial agents against LPC-induced hemolysis. Neither vitamin E nor clarithromycin attenuated hypotonic hemolysis (60 mM NaCl) at concentrations that inhibit LPC-induced hemolysis. On the other hand, both vitamin E and clarithromycin affected LPC micelle formation, suggesting that these drugs directly bind to LPC. We therefore believe that the protective effects of clarithromycin on LPC-induced hemolysis may be related physicochemically to its high lipophilicity and 14-membered ring lactone structure, which help maintain erythrocyte membrane integrity by preventing LPC micelle formation. These drugs likely do not act by a mechanism that protects against osmotic imbalance.
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